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氟伐他汀对急性心肌梗死大鼠基质金属蛋白酶9表达的影响
引用本文:常纯,马兰,王旭红. 氟伐他汀对急性心肌梗死大鼠基质金属蛋白酶9表达的影响[J]. 中国动脉硬化杂志, 2009, 17(2): 85-88
作者姓名:常纯  马兰  王旭红
作者单位:哈尔滨医科大学附属第一医院心内科,黑龙江省哈尔滨市,150086
摘    要:
目的 观察氟伐他汀对急性心肌梗死大鼠基质金属蛋白酶9表达的影响,以探讨他汀类药物改善急性心肌梗死后左心室重构的机制.方法 选用雄性Wistar大鼠47只,随机分为心肌梗死组、心肌梗死用药组、假手术组和假手术用药组,结扎大鼠冠状动脉前降支建立心肌梗死模型,术后心肌梗死用药组及假手术用药组饲氟伐他汀10 mg/(kg·d),心肌梗死组和假手术组不给予任何处理和干预.4周后测左心室血流动力学参数、左心室重量指数及基质金属蛋白酶9含量.结果 术后基质金属蛋白酶9含量和左心室舒张末压在假手术组和假手术用药组均较低,且组间无明显差别(P0.05),在心肌梗死组和心肌梗死用药组均高于假手术组(P<0.05),而在心肌梗死组又高于心肌梗死用药组(P<0.05).与假手术组比较,心肌梗死组和心肌梗死用药组大鼠左心室收缩压、左心室压最大上升速率及左心室压最大下降速率均明显下降(P<0.05),且心肌梗死组较心肌梗死用药组下降更明显(P<0.05).各组左心室重量指数无明显差别(P0.05).结论 氟伐他汀能抑制基质金属蛋白酶9的表达,从而阻止大鼠心肌梗死后心室重构,改善心脏功能.

关 键 词:氟伐他汀  急性心肌梗死  心室重构  基质金属蛋白酶9
收稿时间:2008-10-29
修稿时间:2009-02-01

Effect of Fluvastatin on Expression of Matrix Metalloproteinase-9 in Rats with Acute Myocardial Infarction
CHANG Chun,MA Lan,and WANG Xu-Hong. Effect of Fluvastatin on Expression of Matrix Metalloproteinase-9 in Rats with Acute Myocardial Infarction[J]. Chinese Journal of Arteriosclerosis, 2009, 17(2): 85-88
Authors:CHANG Chun  MA Lan  and WANG Xu-Hong
Affiliation:1.Department of Geriatrics,Second Affiliated Hospital of Harbin Medical University; 2.Department of Cardiology,First Affiliated Hospital of Harbin Medical University,Harbin 150086,China
Abstract:
Aim To observe the influence of fluvastatin on expression of matrix metalloproteinase-9 (MMP-9) in rats with acute myocardial infarction (AMI) and to investigate the mechanism of statin on improving left ventricular remodeling after acute myocardial infarction. Methods 47 healthy male Wistar rats were randomly divided into AMI group,AMI+fluvastatin group,the sham-operated group (sham) and the sham-operated+fluvastatin group. AMI was established by ligation of the anterior descending coronary artery in rats,fluvastatin was fed to AMI+ fluvastatin group and sham+ fluvastatin group by 10 mg/(kg·d) for 4 weeks while the AMI group and the sham group left untreated,then the hemodynamic parameters and mass index of left ventricular and the expression of matrix metalloproteinase-9 were detected. Results The expression of matrix metalloproteinase-9 and left ventricular end-diastolic pressure (LVEDP)were low in the sham-operated group and the sham-operated+fluvastatin group,and there were no significant difference ( P>0.05). Compared with the shams,the production of matrix metalloproteinase-9 and left ventricular end-diastolic pressure were all increased in the AMI group and AMI+ fluvastatin group (P<0.05),and these indexes were increased significantly in the AMI group than those in the AMI+ fluvastatin group (P<0.05). Compared with the sham-operated group and the sham-operated+fluvastatin group,left ventricular systolic pressure(LVSP) and the maximal rate of rise and fall (±dp/dtmax)of left ventricular pressure in the AMI group and AMI+ fluvastatin group were all decreased (P<0.05),moreover,these indexes decreased significantly in AMI group than those in AMI+ fluvastatin group (P<0.05). The mass index of the left ventricular in each group showed no significant difference ( P>0.05). Conclusions Fluvastatin can inhibit the expression of matrix metalloproteinase-9 to prevent ventricular remodeling after acute myocardial infarction in rats and improve cardic function.
Keywords:Fluvastatin   Acute Myocardial Infarction   Ventricular Remodeling   Matrix Metalloproteinase-9
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